Conditional calcineurin knockout mice exhibit multiple abnormal behaviors related to schizophrenia
Open accessAbstract
Calcineurin (CN), a calcium- and calmodulin-dependent protein phosphatase, plays a significant role in the central nervous system. Previously, we reported that forebrain-specific CN knockout mice (CN mutant mice) have impaired working memory. To further analyze the behavioral effects of CN deficiency, we subjected CN mutant mice to a comprehensive behavioral test battery. Mutant mice showed increased locomotor activity, decreased social interaction, and impairments in prepulse inhibition and latent inhibition. In addition, CN mutant mice displayed an increased response to the locomotor stimulating effects of MK-801. Collectively, the abnormalities of CN mutant mice are strikingly similar to those described for schizophrenia. We propose that alterations affecting CN signaling could comprise a contributing factor in schizophrenia pathogenesis.
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Mouse models have shown that a number of proteins associated with glutamate receptors, some of which are directly linked with schizophrenia susceptibility genes, have been suggested to show modifications in patients, which in turn cause schizophrenia-like phenotypes.
“Interestingly, mouse models have shown that a number of proteins associated with glutamate receptors, some of which are directly linked with schizophrenia susceptibility genes, have been suggested to show modifications in patients, which in turn cause schizophrenia-like phenotypes.86,87”
From Glutamate in Schizophrenia: A Focused Review and Meta-Analysis of 1H-MRS Studies (2013) · cites this paper as [87]
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- Authors
- Miyakawa, T., Leiter, L. M., Gerber, D. J., Gainetdinov, R. R., Sotnikova, T. D., Zeng, H., Caron, M. G., & Tonegawa, S.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-07-08
- Volume
- 100
- Issue
- 15
- Pages
- 8987-8992
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC166425
- OpenAlex
- W1963956528
- Cited by
- 489
- References
- 49
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 8 · 2023: 10 · 2022: 12 · 2021: 19 · 2020: 12 · 2019: 17 · 2018: 15 · 2017: 17 · 2016: 24 · 2015: 17 · 2014: 23 · 2013: 34 · 2012: 22
- FWCI
- 16.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health
- RIKEN
- National Institute of Mental Health (MH58880-03, P50MH058880)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- calcineurin, conditional knockout mice, schizophrenia, working memory, prepulse inhibition, latent inhibition, locomotor activity, social interaction, MK-801, NMDA receptor, behavioral abnormalities, schizophrenia pathogenesis
- MeSH terms
- Amphetamine, Animals, Behavior, Animal, Corpus Striatum, Disease Models, Animal, Dopamine, Humans, Male, Mice, Inbred C57BL, Motor Activity, Schizophrenia, Social Behavior, Signal Transduction, Dizocilpine Maleate, Mice, Knockout, Glutamic Acid, Calcineurin, Mice
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